Lysophosphatidylethanolamine (LPE) is generated by PLA2 enzyme, which hydrolyzes the 2nd acyl chain of phosphatidylethanolamine (PE) that is one of the phospholipids forming a cell membrane, and it is present in a small amount in a living body. It has been found that a treatment of LPE can suppress aging of a plant and promote ripening of a fruit (U.S. Pat. No. 5,110,341 and U.S. Pat. No. 5,126,155) and can enhance plant health, protect plants from biotic and abiotic stress-related injuries and enhance the recovery of plant injured as a result of such stresses (U.S. Pat. No. 6,559,099). LPE is mainly produced by treating phosphatidylethanolamine extracted from egg yolk or soy bean with PLA2 enzyme, and the compositional component of LPE is mostly LPE 16:0 and LPE 18:0 in which the 1st acyl chain is 16:0 or 18:0. During the process of studying the biological mechanism related to the suppression of aging caused by LPE, it was found that LPE18:1 is a superior molecule which has much higher biological efficacy than LPE 16:0 or LPE 18:0 (U.S. Pat. No. 6,426,105). At present moment, the technique related to the method for producing LPE uses egg yolk or soy bean as a source material so that the component is mostly LPE 16:0 and LPE 18:0 with almost total absence of LPE18:1 (Korean Patent Registration No. 0331932). Accordingly, efforts have been made to find a source material for producing LPE18:1 but to no avail.
In this regard, it is found according to the present invention that the source material (PE containing the 1st acyl chain of 18:1) for producing LPE18:1 is present in a microorganism like Pseudomonas. The discovery of the source material for producing LPE18:1, and the methods and results of the study are described hereinbelow. Once a plant is infiltrated by a pathogen, a disease-resistant response against part of the pathogen is exhibited by the plant. However, the mechanism related to such response is not clearly known yet. In particular, there is not much information available for the signal transduction mechanism for inducing initial disease resistance. It has been known that, when Pseudomonas syringae pv. tomato DC3000 carrying avrRpm1 (hereinbelow, described as Pst-avrRpm1) invades an extracellular space of Arabidopsis thaliana (Col-0 ecotype) as a host plant, Avr protein (avrRpm1) is introduced by the pathogen to the cytoplasm of a host through the Type III secretion mechanism. It is known that, if the host cell has RPM1, which is a Resistance protein capable of recognizing avrRpm1 protein, the interaction between those proteins causes an increase in salicylic acid, activation of NPR1 (NON-EXPRESSER OF PR GENES 1), and an immune response for inducing resistance genes like expression of PR (PATHOGENESIS RELATED). However, the upper-level molecule for connecting such gene—for gene interaction, genetic basis, and host immune response for inducing plant resistance genes remain mostly unknown.
According to a study regarding the initial signal transduction that is yet to be known, inventors of the present invention found that LPE18:1 is a signaling molecule to induce disease resistance of a plant. It is surprisingly found that LPE18:1 is mainly produced from an invading pathogen (i.e., Pseudomonas). Briefly, the study result indicates that, as Arabidopsis thaliana is attacked by non-pathogenic Pseudomonas (Pst-avrRpm1), intracellular injection of avrRpm1 protein into plant host cells is yielded, and at that time, the protein factor is recognized as a gene-for-gene interaction by the plant and phospholipase A2-alpha (PLA2α) protein is immediately expressed. PLA2α protein is secreted to an extracellular region, in which invading pathogens are present, and it decomposes phosphatidylethanolamine present in pathogen membrane to produce LPE18:1 as a main component. This LPE18:1 exhibits an activity of a signaling molecule and, according to propagation to the surrounding, it enters neighboring cells not infected by the pathogen to induce disease resistance.
As it is shown by the study result described above, it was possible to recognize that the source material (PE containing the 1st acyl chain of 18:1) for producing LPE18:1 is present in a microorganism like Pseudomonas. Thus, the inventors of the present invention carried out large-scale culture of Pseudomonas bacteria, and according to extraction of lipids therefrom and treatment with PLA2 enzyme, confirmed production of a large amount of LPE18:1. The LPE18:1 produced by the inventors was applied to a plant, and the biological effect is compared with a known mixture liquid of LPE 16:0/LPE 18:0 and also with commercially available LPE18:1 of high purity. LPE produced by the inventors using the microorganism Pseudomonas is found to be mostly consisting of LPE18:1 and LPE 16:0 with extremely small amount of LPE 16:1. In terms of the effect, crude LPE18:1 mixture with LPE16:0 produced by the inventors is superior to LPE 16:0/LPE 18:0 mixture. However, it was inferior to pure LPE18:1. Investigation is also made to see whether or not a source material for producing LPE18:1 can be obtained from a microorganism other than Pseudomonas. In this regard, as a result of analyzing phospholipids after separating them from Escherichia coli as Gram negative bacteria, Bacillus subtilis and Arthrobacter citres as Gram positive bacteria, Saccharomyces cerevisiae as yeast, and Chlorella vulgaris as algae, it is found that, according to the treatment with PLA2, LPE18:1 is produced hardly from other microorganisms but only from Pseudomonas. 
Meanwhile, “methods of enhancing plant health, protecting plants from biotic and abiotic stress related injuries and enhancing the recovery of plants injured as a result of such stresses” is described in Korean Patent Application Publication No. 2002-0086604, and “a composition and a method for immunizing plants against diseases” is disclosed in Korean Patent Application Publication No. 1997-0001484. However, the method for producing LPE18:1 from a microorganism of Pseudomonas sp. as described in the present invention has not been disclosed before.